The Depressive Feedback Loop

As I'm sure you have guessed if you have stopped by lately, I am in the depressive phase of my bipolar cycle, and in one which the medications are having less effect than usual moderating. I have been so now for more than a week. I strongly suspect that bipolarity is an abnormality in some kind of natural biological feedback mechanism. For the effect of my recent gallbladder operation appears to be tangled up in this particularly strong swing of my mood. We have all heard the term "post-partum depression", which is almost certainly a feedback mechanism of this sort, a means of forced convalescing after the stress induced dumping of adrenalin and endorphins into the blood stream.

Bipolar disease itself may be an exaggeration of this. Perhaps the initial change occurs when someone half-consciously, perhaps for years and years, "burns the candle at both ends" for the high it induces. When I did a lot of lecturing to college students, I remember the process of starting almost every lecture as a species of low grade focused stage fright, which I always used to prime the pump of words for rhetoric and vivid vocabulary when speaking extempore, and to feed the acting reflex into projecting an image of balanced judgment, knowledge, and confidence. For even if I was all of these about a subject when talking to anyone at a face to face distance, projecting such an image to students in the last row of seats in a large lecture hall requires real acting histrionics, and every time I lectured, I was playing myself.

I also remember quite clearly that a really good lecture left me far more than merely satisfied with my performance. It left me flying higher than a kite. Lecturing 3-4 times a week to large audiences, and constantly getting high from it, may actually have permanently altered the biochemistry of my brain. It bothers me that human neuroscience seems to pay far less attention to the anecdotal reports of people like me than it should. It seems to me that human self-observation of this kind could generate all sorts of fruitful avenues for research. To test my own hypothesis is beyond my competence. I wouldn't have a clue where to start for research and experimental design, but anyone out there who does have a clue is welcome to use the observation above for free and without credit. If it led to better bipolar management, that would be satisfaction enough.

For both my highs and my lows exhaust me as age, nagging minor illnesses, and weight have caught up with me.

In a similar manner, though I don't follow it closely enough to present this as an assured conclusion, it seems to me that there is some sort of correlative brain biochemistry process to the "obesity epidemic" and the corresponding increase among us of Type II diabetes. I am both Type II and obese. For the record, 5' 7" and 272 lbs the day before I went into surgery.

Oddly enough, I don't seem to look it. The anesthesiologist was startled when I gave him those figures, and one would presume he was used to what fat people look like when covered by hospital gowns that hardly flatter one's figure. I do, however, have an exaggerated upper body type from the years I spent in cabinet making immediately before my mental decline. This may explain some of it.

Working in crowded cabinet shops forces a constant style of heavy lifting and toting, with frequent, weight-bearing, twists and turns of the upper body to the right or the left. This process overdevelops the triceps, the deltoids, the upper back, and the shoulders in relation to the rest of the body. Everybody in a shop sooner or later develops some variation of this body type. A chronic complaint among us was finding shirts that didn't bind us across the back and upper arms. Besides needing size 2x-3x to cover my chest and stomach, I still have this problem.

But, be that as it may, Type II diabetes got me into the habit of looking at food labels. By doing so, and by altering my diet, I have so far avoided the need of any medication to control my blood sugar levels. When I started looking carefully at labels, I found something which I strongly suspect may be one of the real bad actors in obesity and Type II--High Fructose Corn Syrup.

For the past fifteen years or so HFCS has been steadily replacing beet and cane sugars in products ranging from soda pop to barbecue sauce. The way in which plain field corn is turned into this designer sweetener is both arcane and complicated, with some of the steps involving biochemical processing by living bacteria, in the way similar to how yeast is used to bake bread. But even with this, most high volume food manufacturers find HFCS to be considerably cheaper to use than cane or beet sugar, and it has proved to be a bonanza for our corn crop based American agriculture.

The next time you come home from the store, do a little label survey and see both just how many times HFCS is ingredient #1, #2, or #3 on the labels, and in what a wide range of products it appears. You will be astonished at the results. Unless we go out of our way to avoid it we consume an unbelievable amount of HFCS daily and were consuming virtually none of it at all before 1990. The correlation to our "obesity epidemic" and the rise of Type II diabetes is frighteningly exact. And my rough and ready empirical observations strongly suggest that HFCS is screwing up the appetite sensing brain biochemistry of people who consume as much of it as most of us do.

Most of you are probably familiar with sodium spices--table salt or MSG--and how they can do this. If you are not, try changing the packaged nuts that you eat from the salted to the unsalted variety. You will very quickly find that your appetitive craving for the nut oil and the nut protein is far more quickly satisfied, with fewer nuts, if the salt is gone.

By purchasing and trying equivalent products with and without HFCS I have come to the conclusion that the processing of it in the body somehow delays the onset of appetitive satisfaction. The clearest case was one of two types of whole grain bread, Pepperidge Farm 15 Grain [a very good product and without HFCS], and a generic variety of equally tasty whole grain bread called Private Selection with HFCS.

The consistent results I have observed in myself is that 20 minutes after eating two slices of Pepperidge Farm each with two pats of butter and one teaspoon of honey, my craving for any more food was completely gone. After the same 20 minutes with two slices of the Private Selection, decorated in the same way, the craving to eat more was still quite strong.

This is perfectly consistent with the known metabolic processes. I am told that, unlike glucose, the maid of all work sugar that actually fuels most of our body, fructose must metabolize exclusively in the liver, with the following consequences:

Fructose does not cause insulin release from beta cells, as these lack fructokinase. One of the results of this is that fructose consumption does not dampen appetite. This may lead to increased caloric intake with obesity and the metabolic syndrome as a result....

So what? Well, some of that fructose winds up as glycogen and glucose. That is ok; we need glucose in the blood. The rest of the fructose rushes through pyruvate, is transferred to mitochondria, and finally converted to fatty acids and exported from the liver as triglycerides.

That fat formation is a major problem. People that consume large amounts of sugar seem to demonstrate increased plasma triglyceride levels. This is quite parallel to eating large quantities of saturated fats. While the mechanisms here are not completely clarified, there is good reason to believe that increased plasma triglyceride are a moment in development of atherosclerosis and CVD....

Our diet through thousands of years included starches as the major carbohydrate source and fructose as a sweet extra in fruits and honey. Remember, progression to the "hunter stadium" came long after development of the first humanoids. A very active conversion of that limited fructose to fructose-1-phosphate (not 6-phosphate) appears to have been elemental in regulation of hepatic glucokinase and glucose metabolism.

The epidemic growth of overweight, diabetes type 2, hypertension and CVD in urban societies around the globe today may well have our exceedingly high sugar consumption as a major underlying factor. We were simply "not made" to eat 25% of our food in the form of sugar.

Thus clearly, I think, we can label HFCS by the more homely and truer name of Pigout Juice.

We are an incredibly complicated bundle of relations between how we feel, what we eat, and how our bodies respond to it. My weight increased by 60 lbs between 2002 and 2005 and another 40 lbs between 1992 and 2002. Both experientially, and objectively in terms of monetary percentage of my food budget, my food consumption did not significantly increase throughout this period and I certainly am not now eating over 30% more food than I was in 1993! What did change to that degree over that period of time is my consumption of High Fructose Corn Syrup.

Since deliberately going out of my way to eliminate HFCS from my diet after being diagnosed as Type II diabetic in 2005, my blood glucose levels have remained well within safe limits from dietary control alone and my weight has dropped from a high of 282 lbs. to a median of somewhere around 265 lbs. with a + or - 7 lb. fluctuation. I suspect that it will take a significant decrease in total caloric intake to push beyond the lower number of this range.

I know empirically that I am also locked in the dilemma where both my bipolar problems and my thyroid problems interact very intimately with my blood sugar levels. Lowering blood sugar, especially runs the risk of magnifying both the manic and the depressive phases. This probably will place a lower limit on how much I will be able to decrease my actual caloric intake in the future.

But I will say that blood sugar control, and some weight loss, combined with an appetite that is far more satisfied and less prone to pigging out, is well worth the trouble of restricting both the salt and the HFCS in one's diet.